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Lactacystin inhibits 3T3-L1 adipocyte differentiation through induction of CHOP-10 expression
- Source :
- Biochemical and Biophysical Research Communications. 350:1-6
- Publication Year :
- 2006
- Publisher :
- Elsevier BV, 2006.
-
Abstract
- Hormonal induction triggers a cascade leading to the expression of CCAAT/enhancer-binding protein(C/EBP)alpha and peroxisome proliferator-activated receptor (PPAR) gamma, C/EBPalpha, and PPARgamma turns on series of adipocyte genes that give rise to the adipocyte phenotype. Previous findings indicate that C/EBPbeta, a transcriptional activator of the C/EBPalpha and PPARgamma genes, is rapidly expressed after induction, but lacks DNA-binding activity and therefore cannot activate transcription of the C/EBPalpha and PPARgamma genes early in the differentiation program. Acquisition of DNA-binding activity of C/EBPbeta occurs when CHOP-10, a dominant-negative form of C/EBP family members, is down-regulated and becomes hyperphosphorylated as preadipocytes traverse the G1-S checkpoint of mitotic clonal expansion. Evidences are presented in this report that lactacystin, a proteasome inhibitor, up-regulated the CHOP-10 expression, blocked the DNA-binding activity of C/EBPbeta, and subsequently inhibited MCE as well as adipocyte differentiation.
- Subjects :
- Lactacystin
Biophysics
Mitosis
Peroxisome proliferator-activated receptor
Biology
Biochemistry
Mice
chemistry.chemical_compound
Downregulation and upregulation
Transcription (biology)
3T3-L1 Cells
Adipocyte
Adipocytes
medicine
Animals
Receptor
Molecular Biology
chemistry.chemical_classification
CCAAT-Enhancer-Binding Protein-beta
Cyclin-Dependent Kinase 2
Cell Differentiation
DNA
Cell Biology
Phenotype
Molecular biology
Acetylcysteine
Up-Regulation
chemistry
Proteasome inhibitor
biological phenomena, cell phenomena, and immunity
Transcription Factor CHOP
Protein Binding
medicine.drug
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 350
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....0eb4554593d583e3e0e8d78985c18606